Cholesterol crystals piercing the arterial plaque and intima trigger local and systemic inflammation

IL-22 is induced by S100/calgranulin and impairs cholesterol efflux in macrophages by downregulating ABCG1

“…Cholesterol crystallization is an after-effect of free cholesterol accumulation within the plaques ( 24,25 ). In macrophages, cholesterol accumulation is regulated by cholesterol uptake via CD36, LOX1, and other receptors, and via cholesterol effl ux regulated by the cholesterol transporter proteins ABCA1 and ABCG1 ( 26,27 ).…”

Lipid crystals mechanically stimulate adjacent extracellular matrix in advanced atherosclerotic plaques

“…Previous studies have reported that solid-state LCs perforated the ECM in extremely vulnerable conditions [13,15]. To further investigate the underlying mechanisms, we studied the spatial correlation between extracellular LCs and ECMs.…”

“…The ability to visualize the fluorescence materials of MPEF can be utilized to image the intrinsic autofluorescence of elastin fibers, and SHG is specialized for visualizing collagen fibrils based on unique structural features [10e12]. Among the diverse range of lipids that compose lipid cores, lipid crystals (LCs) have recently been perceived as a factor that induces both local and systemic inflammation leading to plaque rupture [13,14]. We previously reported some microanatomical features of atherosclerotic lesions and characterized four major types of atherosclerotic lipids, including two distinct types of LCs, based on multiplex CARS analysis [15].…”

Original article Circulated CD4 + CD28 - lymphocytes rate and their cytotoxicity and morphological parameters of internal carotid artery atheromatous plaques in patients with atherosclerosis-related ischemic stroke

“…Cholesterol crystals within atherosclerotic lesions are recognized as a potent factor promoting inflammation in the wall of an arterial vessel, which results in a cascade of events leading to plaque destabilization [1,4,25]. Other researchers suggest that CD4 + CD28 -Lc appear originally in the blood and then infiltrate tissues, including atheromatous lesions, in which they enhance inflammatory mechanisms [27].…”